1981
DOI: 10.1037/h0077801
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Disruption of appetite but not hunger or satiety following small lesions in the amygdala of rats.

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Cited by 44 publications
(24 citation statements)
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References 44 publications
(55 reference statements)
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“…This ''within group'' comparison controls for many sources of variability, which is an advantage when small sample sizes are studied (Zolman, 1993;Rasia-Filho and Lucion, 1996;de Castilhos et al, 2006). However, these novel data did not provide strong evidence that the MePD would be contributing to direct goal-oriented feeding behavior or hunger and polyphagia (Schoenfeld and Hamilton, 1981;Rollins et al, 2006). In addition, there are few data to support an involvement of the MeA subnuclei with learning of appetitive motivated tasks such as drinking of taste solutions or eating more palatable food (reviewed in Knapska et al, 2007).…”
Section: Discussionmentioning
confidence: 98%
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“…This ''within group'' comparison controls for many sources of variability, which is an advantage when small sample sizes are studied (Zolman, 1993;Rasia-Filho and Lucion, 1996;de Castilhos et al, 2006). However, these novel data did not provide strong evidence that the MePD would be contributing to direct goal-oriented feeding behavior or hunger and polyphagia (Schoenfeld and Hamilton, 1981;Rollins et al, 2006). In addition, there are few data to support an involvement of the MeA subnuclei with learning of appetitive motivated tasks such as drinking of taste solutions or eating more palatable food (reviewed in Knapska et al, 2007).…”
Section: Discussionmentioning
confidence: 98%
“…The feeding behavior of homeostatically challenged, food-deprived rats having a self-selection macronutrient diet is the resultant of serial and parallel neural connections needed for processing multiple sensorial information, metabolic/hormonal internal demands, and organization of behavioral displays (Schoenfeld and Hamilton, 1981;Newman, 1999;Berthoud, 2002). However, the influence of the MePD upon different hypothalamic nuclei that control neuroendocrine secretion or behavior display is far from simple.…”
Section: Discussionmentioning
confidence: 99%
“…Besides hypothalamic regions, GLP-1 has also been shown to be present in the amygdala (15), which does not only provide afferent neuronal input to the hypothalamus via the amygdalofugal pathway (21) but also may play a role in the regulation of ingestive behavior (3,9,42). At the extrahypothalamic region of the amygdala, however, GLP-1 was not able to alter feeding behavior.…”
Section: Glp-1 and A High Density Of Glp-1 Receptors Havementioning
confidence: 97%
“…Within the hypothalamus, GLP-1-containing nerve fibers and terminals have been shown to be located in the paraventricular nucleus of the hypothalamus (PVN), the ventromedial hypothalamus (VMH), dorsomedial hypothalamus (DMH), and lateral hypothalamus (LH), well known as integrative areas for feeding regulation (12,15,23). In addition, GLP-1 is also present in the amygdala (15), a brain region providing neuronal input to the hypothalamus and participating in the regulation of ingestive behavior (3,9,21,42). In all these areas, the presence of GLP-1 receptors has recently been demonstrated (11).…”
mentioning
confidence: 99%
“…Norgren [1976], who recorded antidromic activation from the vicinity of the central nucleus to gustatory units in the pons, hypothesized that this amygdaloid region acts as a relay for taste information. This rich sensory innervation provides a neuroanatomical correlate to the notion that the amygdala primarily mediates the appetite experience, but is without influence on hunger and body weight regulation [Schoenfeld and Hamilton, 1981]. The medial posterodorsal and central amygdaloid nuclei are further innervated from the arcuate nucleus [Ottersen, 1980;Broberger et al, 1998a], and also here are CART-ir neurons closely apposed by NPY-ir terminals [Broberger, 1999].…”
Section: Mesolimbic Structures and The Amygdalamentioning
confidence: 89%